Summary: This paper investigates a haptotactic cross-diffusion model \[ \begin{cases} c_t = D_c \Delta c - \eta_c \nabla \cdot (c \nabla u) + \mu_1 c - \mu_1c^\gamma - \rho c v - \kappa c i, \\ i_t = D_i \Delta i - \eta_i \nabla \cdot (i \nabla u) + \rho c v + p_0 \kappa c i - \delta_i i, \\ s_t = D_s \Delta s - \eta_s \nabla \cdot (s \nabla u) + \left(1-p_0\right) \kappa c i - \delta_s s, \\ u_t = -u \left(\alpha_c c + \alpha_i i + \alpha_s s \right) + \mu_2 u(1-u), \\ v_t = D_v \Delta v - \eta_v \nabla \cdot(v \nabla u) + b_i i + b_s s - \rho c v - \delta_v v \end{cases} \] in a bounded domain \(\Omega \subset \mathbb{R}^2\) with smooth boundary. The model highlights the impact of syncytia formation triggered by fusogenic oncolytic virus on therapeutic efficacy, in addition to the influence of the extracellular matrix (ECM) taxis over the tumor-oncolytic virus interactions. It is proved that under appropriate structural assumptions on the system parameters and sufficiently smooth initial data, the model possesses one global bounded solution.